Infections of the facial spaces

1. Infections of the
facial spaces
PRESENTED BY: DR. MOSTAFA OSAMA
DR. ABRAR ISMAEEL
DR. FATIMA THAMER
UNDER THE SUPERVISION OF DR. ASMAA

2. Odontogenic infections
 Orofacial infections may be odontogenic or non odontogenic in nature
and the vast proportion of odontogenic infections are caused by the
endogenous bacteria present in the oral cavity.
 Examples of odontogenic infections are periapical and periodontal
infections. Most of non-odontogenic infections are associated with an
underlying medical condition.
 Examples of non-odontogenic infections are that of the skin, tonsils, or
maxillary sinuses. Occasionally, infections could develop following an
anesthetic injection or a surgical procedure

3. Odontogenic infections
 One of the most difficult problems to manage in dentistry is odontogenic
infections.
 These infections may range from low-grade, well-localized infections that
require only minimal treatment to severe life-threatening facial space
infection

4. Odontogenic infections
 The predisposition of an infection is related to an interruption of the fine
balance between the host, the micro-organism and the environment.
 This imbalance, in turn, may lead to the multiplication of micro-organisms
followed by invasion of different structures.
 The severity of infection is related to the number and virulence of micro-
organisms and resistance of the host

5. Odontogenic infections
 Odontogenic infections are typically Polymicrobial.
 The most common species of bacteria isolated in odontogenic infections
are the anaerobic gram-positive cocci Streptococcus milleri group and
Peptostreptococcus, anaerobic gram-negative rods, such as Bacteroides
(Prevotella) also play an important role. Aerobic bacteria has little effect

6. Stages of Odontogenic infections
 Odontogenic infections progress through 3 stages: inoculation, cellulitis
and abscess . Sinus tract/fistula may be seen in neglected cases
 Inoculation:
 Is characterized by the entry of pathogenic microbes into the body without
disease occurring. An infection involves the proliferation of microbes resulting
in triggering of the defense mechanism, a process manifesting as inflammation

7. Stages of Odontogenic infections
 Cellulitis:
 Is an acute diffuse painful indurated swelling of the soft tissues resulting from a
diffuse spreading of purulent exudate along the fascial planes with or without
suppuration
 Abscess:
 A collection of pus in a cavity formed by disintegration of tissue as result of
infection
 Discharging Sinus:
 Some times abscess ruptures to produce a draining sinus tract. Usually, infection
recur when the site of drainage closes. Sinus is thus a one side tract of a single
compartment

9. Stages of Odontogenic infections
 Fistulae:
 A drainage pathway or abnormal communication between two epithelium-lined
surfaces due to destruction of the intervening tissue. Fistula is thus an
epithelialized tract opening in both side of two different compartment

10. Acute dentoalveolar abscess
 The usual cause of odontogenic infections is necrosis of dental pulp, which
is followed by bacterial invasion through the pulp chamber and into the
deeper tissues.
 Necrosis of the pulp is the result of deep caries of a tooth, to which the
pulp responds with a typical inflammatory reaction.
 Vasodilatation and edema cause pressure in the tooth and severe pain as
the rigid walls of the tooth prevent swelling.
 If left untreated the pressure leads to strangulation of the blood supply to
the tooth through the apex and consequent necrosis

11. Acute dentoalveolar abscess
 The necrotic pulp then provides a perfect
setting for bacterial invasion into the bone
tissue.
 Pus is formed in the cancellous bone,
and spreads in various directions by way
of the tissues presenting the least resistance
until a cortical plate is encountered.

12. Acute dentoalveolar abscess
 Clinically, the condition has rapid onset.
 Radiographically, changes in bone density may not be noticeable (you
have to wait for approximately 10 days to detect bone rarefaction).
 It is characterized by symptoms that are classified as local and systemic.
 Local symptoms:
 Pain:
 The severity of the pain depends on the degree of inflammation. Initially, the pain is
dull and continuous and worsens during percussion of the responsible tooth or when
it comes into contact with antagonist teeth. There is a sense of elongation of the
responsible tooth and slight mobility

13.  Edema:
 Edema appears intraorally or extraorally and it usually has a buccal and more
rarely palatal or lingual localization.
 This swelling presents before suppuration, particularly in areas with loose
tissue, such as the sublingual region, lips, or eyelids.
 Usually the edema is soft with redness of the skin.
 During the final stages, the swelling fluctuates, especially at the mucosa of the
oral cavity.
 This stage is considered the most suitable for incision and drainage of the
abscess.

14.  Systemic Symptoms:
 The systemic symptoms usually observed are: fever, chills, malaise with pain in
muscles and joints, insomnia, nausea, and vomiting.
 Laboratory tests usually show leukocytosis, an increased erythrocyte
sedimentation rate, and a raised C-reactive protein (CRP) level
 Treatment:
 Extraction of the tooth (or removal of the necrotic pulp by an endodontic
procedure) results in resolution of the infection

15. Spread of odontogenic infection
 Routes of Spread of Odontogenic Infection:
 a. By direct continuity via the tissue
 b. Via the lymphatics into the regional lymph nodes and subsequently into the
blood stream
 c. Haematogenous spread leading to thrombophlebitis, bacteremia or
septicemia. Thrombus may propagate along the veins, entering the cranial
cavity via emissary veins to produce cavernous sinus thrombosis

16. Direct spread
 Whether the pus spreads buccally, palatally or lingually depends mainly on
the position of the tooth in the dental arch, the thickness of the bone, and
the distance it must travel

17. Direct spread
 The length of the root and the relationship between the apex and the
proximal and distal attachments of various muscles also play a significant
role in the spread of pus

18. Fascial space infections
 Sometimes, infection may spreads towards the fascial spaces, forming
serious abscesses called fascial space infection.
 The fascial spaces are potential areas and do not exist in healthy
individuals.
 Bone, muscle, fascia, neurovascular bundles, and skin can all act as barriers
to the spread of infection.
 It should be remembered however, that no tissue barrier or boundary is so
restrictive to universally prevent spread of infection into contiguous
anatomical spaces

19. Fascial space infections
 Fascial space infection
 Facial spaces have been classified as either primary or secondary spaces infection
 Primary maxillary spaces
 Canine
 Buccal
 Infratemporal
 Primary mandibular spaces
 Submental
 Buccal
 Submandibular
 Sublingual
► Secondary fascial spaces
► Masseteric
► Pterygomandibular
► Superficial and deep temporal
► Lateral pharyngeal
► Retropharyngeal
► Prevertebral

20. Primary maxillary spaces
 Canine Space
 It is the region between anterior surface of
maxilla and overlying levator muscles of upper
lip.
 Contains angular artery & vein, infraorbital
nerve.
 Etiology-
 Maxillary canine & first premolar infection &
sometimes mesiobuccal root of first molars.
 Boundaries:
 Superiorly: levator superioris alaque nasi and
levator labii superioris
 Inferiorly: caninus muscle
 Medially: anterolateral surface of maxilla
 Posteriorly: buccinator mucsle
 Anteriorly: orbicularis oris

21. Canine Space
 Clinical Features:
 Swelling of cheek, lower eyelid & upper lip.
 Drooping of angle of mouth.
 Nasolabial fold obliterated.
 Odema of lower eyelid

22. Buccal Space
 Boundaries:
 Superiorly: zygomatic arch.
 Inferior: inferior border of mandible.
 Laterally: skin & subcutaneous tissue.
 Medially: buccinator muscle, buccopharyngeal fascia.
 Posteriorly: anterior edge of masseter muscle.
 Anteriorly: posterior border of zygomatious major &
depressor anguli oris.
 Contents:
 Buccal fat pad.
 Stenson's duct.
 Facial artery.

23. Buccal space
 Etiology:
 Infected mandibular & maxillary premolars
& molars.
 Clinical Features:
 Obliteration of nasolabial fold.
 Angle of mouth shifted to opposite side.
 Swelling in check extending to corner of
mouth.
 Buccal space associated with temporal space
- Dumb bell shaped appearance due to lack
of swelling over zygomatic arch.

24. Infratemporal Space
 Boundaries:
 Superiorly: infratemporal surface of greater wing of
sphenoid.
 Inferiorly: lateral pterygoid muscle.
 Laterally: temporalis tendon & coronoid process.
 Medially: lateral pterygoid plate & lateral pharyngeal wall.
 Posteriorly: condyle & lateral pterygoid muscles.
 Anteriorly: infratemporal surface of maxilla & posterior
surface of zygomatic bone.
 Contents:
 Pterygoid plexus of veins.
 Internal maxillary artery.
 Mandibular nerve & its branches.

25. Infratemporal Space
 Etiology:
 Infected maxillary third molars.
 Infected needles or contaminated LA solution.
 Clinical Features:
 Extra-oral swelling over sigmoid notch area.
 Intra-oral swelling in tuberosity area.
 Trismus.
 Spread of Infection:
 To temporal space.
 Cavernous sinus thrombosis- infection spreads via
pterygoid plexus of veins.

26. Primary mandibular spaces
 Submental Space
 Boundaries:
 Roof: mylohyoid muscle.
 Inferior: deep cervical fascia, platysma,
superficial fascia & skin
 Laterally: anterior belly of digastric.
 Posteriorly: submandibular space.
 Contents:
 Lymph nodes
 anterior jugular vein.

27. Submental Space
 Etiology:
 Infected mandibular incisors.
 Anterior extension of submandibular
space.
 Clinical Features:
 Chin appears glossy & swollen.
 Pain & discomfort on swallowing.

28. Submandibular Space
 Submandibular Space
 Boundaries-
 Superiorly: mylohyoid muscle, inferior border of
mandible.
 Inferior: anterior & posterior belly of digastric.
 Laterally: deep cervical fascia, platysma, superficial
fascia & skin.
 Medially: hyoglossus, styloglossus, mylohyoid muscle.
 Posteriorly: to hyoid bone.
 Anteriorly: submental space.

29. Submandibular Space
 Contents:
 Submandibular salivary gland.
 Proximal portion of Wharton's
duct.
 Lingual & hypoglossal nerves.
 Branches of facial artery -
palatine, tonsillar,
glandular,submental.

30. Submandibular Space
 Etiology:
 Infected mandibular 2nd & 3rd molars.
 Clinical Features:
 Indurated swelling in submandibular region.
 Usually bulges over lower border of mandible.
 Spread of Infection:
 Across midline to contralateral space.
 To contiguous pharyngeal spaces.

31. Sublingual Space
 Boundaries:
 Superiorly: mucosa of floor of
mouth.
 Inferior: mylohyoid muscle.
 Posteriorly: body of hyoid bone.
Anteriorly & laterally: inner
aspect of mandibular body.
 Medially: geniohyoid,
styloglossus, genioglossus
muscle.

32. Sublingual Space
 Contents:
 Deep part of Submandibular
gland.
 Wharton's duct.
 Sublingual gland.
 Lingual & hypoglossal nerves.
 Terminal branches of lingual
artery.

33. Sublingual Space
 Etiology:
 Infected mandibular premolar &
first molar.
 Clinical Features:
 Swelling of floor of mouth.
 Elevated tongue.
 Pain & discomfort on swallowing.

34. Secondary Fascial Spaces
 Masseteric Space
 Boundaries:
 Superiorly: zygomatic arch.
 Inferiorly: inferior border of mandible.
 Laterally: masseter muscle.
 Medially: ramus of mandible.
 Posteriorly: parotid gland & its fascia.
 Anteriorly: buccal space & buccopharyngeal fascia.
 Contents-
 Masseteric artery & vein.
 Etiology:
 Mandibular third molars (pericoronitis)

35. Pterygomandibular Space
 Boundaries:
 Superiorly: lower head of lateral
pterygoid muscle.
 Laterally: medial surface of ramus.
 Medially: medial pterygoid muscle.
 Posteriorly: deep part of parotid.
Anteriorly: pterygomandibular raphe.
 Contents:
 Inferior alveolar neurovascular bundle.
 Lingual & auriculotemporal nerves
 Mylohyoid nerve & vessels.

36. Pterygomandibular Space
 Etiology:
 Infected mandibular third
molars(mesioangular/horizontal)
 Pericoronitis.
 Infected needles or contaminated LA
solution.
 Clinical Features:
 Absence of extra-oral swelling.
 Severe trismus.
 Difficulty in swallowing
 Anterior bulging of half of soft palate &
tonsillar pillars with deviation of uvula to
unaffected side.
 Spread of Infection:
 Superiorly to infratemporal space.
 Medially to lateral pharyngeal space.
 To submandibular space.

37. Lateral Pharyngeal Space
 Boundaries-
 Shape of an inverted cone or pyramid, the
base is at sphenoid bone and the apex at
hyoid bone.
 Anteriorly: pterygomandibular raphe.
 Posteriorly: extends to prevertebral fascia.
 Laterally: fascia covering medial pterygoid
muscle, parotid & mandible.
 Medially: buccopharyngeal fascia on lateral
surface of
 superior constrictor muscle. Styloid process
divides the space into anterior muscular and
 posterior vascular compartment.

38. Ludwig’s Angina
 Ludwig's Angina is a massive
indurated brawny cellulites
 Occurs bilaterally in the
submandibular, sublingual &
submental spaces.
 Infection is propagated by lymphatic
spread or directly through
submandibular space.
 Cellulitis is then rapidly spread to
involve bilaterally the
parapharyngeal and pterygoid
spaces

39. Ludwig’s Angina
 Clinically, the condition is characterized by:
 Painful bilateral swelling of floor of mouth and elevation of tongue.
 Bilateral firm, brawny painful, diffuse swelling of upper part of neck
 Difficulty in swallowing and breathing
 Rapid pulse, high fever, fast respiration
 Leucocytosis
 Patient should be hospitalized.
 Conservative treatment includes intravenous antibiotic therapy and
close airway observation.
 Pus is evacuated, when indicated, by through & through drainage

40. Cavernous Sinus Thrombosis
 Infections may spread via hematogenous route to the cavernous sinus
occurs from:
 Anteriorly:
 Superior labial venous plexus to
 Anterior facial vein, then via
 Superior or inferior ophthalmic vein into the cavernous sinus
 Posteriorly:
 from retromandibular vein to the ptrygo-mandibular venous plexus
 the emissary vein passing through foramen ovale, spinosum, to cavernous sinus
 Superior petrosal sinus (inside the ear)

41. Cavernous Sinus
Thrombosis
Anterior pathway
ophtalmic v.
infraorb. v.
deep facial v.
Posterior pathway
pterygoid plx. → oval or spinosum foramen

42. Evaluation of patient with dentofacial
infections
 Patients with dentofacial infections may present with various signs and symptoms, ranging from
less important to extremely serious.
 Quick assessment of the patient’s situation is essential as the first step of therapy.
 If the patient shows central nervous system changes, airway compromise, or toxification, then
immediate hospitalization, aggressive medical treatment, and surgical intervention may be
necessary.
 Basic principles of patient evaluation must be followed.
 A complete patient history
 physical examination,
 laboratory investigation,
 radiological investigation,
 and accurate and appropriate interpretation of findings must be made.
 Following these basic principles provides the best chance of accurate diagnosis and treatment

43. Principles of treating infection
 Proper knowledge of anatomy, anatomical landmarks and vital structures
of the face and neck is necessary to predict pathways of spread of
infections and to drain these spaces
 Remove the cause (i.e. extract the tooth, open & extirpate the pulp)
 Incision & Drainage (never let the sun set on undrained pus)
 Antibiotics

44. Incision and Drainage
 For intraoral abscess, stab incision is done through the mucosa down deep to the underlying bone.
 Incisions for extra-oral abscesses should be placed in a skin crease to leave the least evident scar.
 Once the skin incision is made, blunt evacuation of pus might be done using a curved haemostat.
 The abscess cavity should be kept open to allow continuous drainage.
 Corrugated rubber, ribbon gauze, or tubular plastic drain might be used.
 Incision and drainage helps to get rid of toxic purulent material, to decompress edematous tissues,
to allow better perfusion of blood, which contains antibiotic and defense elements, and to increase
oxygenation of the infected area

45. Antibiotic Therapy in orofacial
infections
 Antibiotics is generally indicated when the swelling is diffuse and spreading, and especially if fever is
present and infection spreads to the fascial spaces, regardless of whether there is an indication of the
presence of pus.
 Antibiotic therapy is usually empiric, given the fact that it takes time to obtain the results from a
culture sample.
 Odontogenic infections are polymicrobial. Historically, penicillins have been used to treat
odontogenic infections.
 ith the ever-increasing bacterial resistance to penicillinbased antibiotics with dental pathogens and
concurrent clinical failures with penicillins, other agents have become increasingly attractive.

46. Antibiotic Therapy in orofacial
infections
 Amoxicillin/clavulanate (augmentin), clindamycin, and metronidazole are useful alternatives in
combating the anaerobic bacteria involved in dentoalveolar infection .
 Clindamycin has more recently become a drug of choice for the management of odontogenic
infections because of the
 bacterial susceptibility to this drug
 great oral absorption
 low emergence of bacterial resistance and
 good antibiotic levels in bone.

47. Criteria for hospitalization
 Rapidly progressive cellulitis
 Dyspnea (shortness of breath or difficult breathing)
 Dysphagia (difficulty in swallowing)
 Spread to deep facial spaces
 Fever of more than 38º C
 Intense trismus ( inter-incisal distance less than 10 mm)
 Failure of initial treatment
 Severe involvement of general health status
 Immunocompromised patients (diabetes, alcoholism or drug addiction,
malnutrition, treatment with corticoids,….)